Chiowchanwisawakit Praveena, Lambert Robert G W, Conner-Spady Barbara, Maksymowych Walter P
University of Alberta, Edmonton, Alberta, Canada.
Arthritis Rheum. 2011 Aug;63(8):2215-25. doi: 10.1002/art.30393.
Focal fat infiltration is frequently visible on magnetic resonance imaging (MRI) of the spine in patients with ankylosing spondylitis (AS) and likely reflects postinflammatory tissue metaplasia. To support the concept of coupling between inflammation and new bone formation, we tested the hypothesis that focal fat infiltration at a vertebral corner is more likely to evolve into a de novo syndesmophyte.
MRI scans were obtained at baseline and radiographs were obtained at baseline and 2 years in 100 AS patients from 2 cohorts: a clinical trial cohort (n = 38) and an observational cohort (n = 62). In the clinical trial cohort, patients were randomized to receive anti-tumor necrosis factor (anti-TNF) therapy or placebo for 12-24 weeks and then open-label treatment for 2 years. In the observational cohort, patients received either standard therapy (n = 36) or anti-TNF therapy (n = 26) for 2 years. Vertebral corner inflammation and fat infiltration were assessed independently by pairs of readers who were blinded with regard to the radiographic findings.
New syndesmophytes developed significantly more frequently in vertebral corners with fat in both the clinical trial (10.2%) and the observational (6.5%) cohort as compared to those without either feature on baseline MRI (3.1% [P = 0.008] and 1.4% [P = 0.0002], respectively). Adjusting for within-patient variations in baseline syndesmophytes/ankylosis, vertebral corners that were fat-positive/inflammation-positive significantly predicted new syndesmophytes, with an odds ratio (OR) of 7.6 (95% confidence interval [95% CI] 1.5-38.5 [P = 0.01]), while a model that included baseline variations in both fat and inflammation showed an OR of 5.8 (95% CI 2.2-15.3 [P < 0.001]) for inflammation and an OR of 1.9 (95% CI 0.9-4.1 [P = 0.1]) for fat.
Our data lend support to the hypothesis that inflammatory lesions evolve into new bone through a process of tissue metaplasia that includes fat infiltration.
在强直性脊柱炎（AS）患者的脊柱磁共振成像（MRI）上，局灶性脂肪浸润经常可见，这可能反映了炎症后组织化生。为了支持炎症与新骨形成之间存在关联的概念，我们检验了以下假设：椎体角的局灶性脂肪浸润更有可能演变成新生的韧带骨赘。
对来自2个队列的100例AS患者在基线时进行MRI扫描，并在基线和2年时拍摄X线片：一个临床试验队列（n = 38）和一个观察性队列（n = 62）。在临床试验队列中，患者被随机分配接受抗肿瘤坏死因子（抗TNF）治疗或安慰剂治疗12 - 24周，然后进行2年的开放标签治疗。在观察性队列中，患者接受标准治疗（n = 36）或抗TNF治疗（n = 26）2年。由对X线片结果不知情的成对阅片者独立评估椎体角炎症和脂肪浸润情况。
与基线MRI上无这两种特征的椎体角相比，在临床试验队列（10.2%）和观察性队列（6.5%）中，有脂肪的椎体角出现新韧带骨赘的频率显著更高（分别为3.1% [P = 0.008]和1.4% [P = 0.0002]）。在校正患者内基线韧带骨赘/强直的变化后，脂肪阳性/炎症阳性的椎体角显著预测了新韧带骨赘，优势比（OR）为7.6（95%置信区间[95%CI] 1.5 - 38.5 [P = 0.01]），而一个同时纳入脂肪和炎症基线变化的模型显示，炎症的OR为5.8（95%CI 2.2 - 15.3 [P < 0.001]），脂肪的OR为1.9（95%CI 0.9 - 4.1 [P = 0.1]）。
我们的数据支持了以下假设，即炎症性病变通过包括脂肪浸润在内的组织化生过程演变成新骨。
